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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with hyperthyroidism, heart failure, and depressed ejection fraction, in whom myocardial damage was evidenced by In111-labelled monoclonal antimyosin antibodies, is presented. Both myocardial damage and left ventricular dysfunction disappeared after antithyroid therapy. This suggests that, in addition to volume overload, heart failure in hyperthyroidism could be also due to the presence of potentially reversible concurrent myocardial damage.
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PMID:Active myocardial damage in hyperthyroidism. A concurrent mechanism of heart failure reversed by treatment. 749 95

The two isomers of the positive inotropic compound EMD 53998, (+)EMD 57033 and (-)EMD 57439, possess selective calcium sensitizing and phosphodiesterase (PDE) inhibitory properties, respectively. We measured the pharmacological responses to both enantiomers in isolated rat cardiac and vascular tissues and in muscles from severely failing human hearts. We also measured positive inotropic and chronotropic responses to EMD 57033 in cardiac tissues from rats with thyroid dysfunction, diabetes, or hypertension. Both compounds increased force of contraction in isolated rat cardiac tissues, although the ventricular response to EMD 57439 was only approximately 10% that of calcium chloride. Forskolin pretreatment potentiated responses to both compounds in atria but only to EMD 57439 in ventricles. Hyperthyroidism increased ventricular responses to EMD 57033 relative to calcium chloride; hypothyroidism and diabetes decreased these responses. Ventricular responses were unchanged in hypertensive rats. Both enantiomers produced positive inotropy in human isolated right atrial trabeculae, although the maximal increases were only 14% (EMD 57033) and 26% (EMD 57439) that of calcium chloride. In rat thoracic aortic rings, both enantiomers produced relaxation; the responses due to EMD 57033 were endothelium dependent. Thus, calcium sensitization produces positive inotropy and vascular relaxation in rats. Positive chronotropic responses to EMD 57033 are most likely due to PDE inhibition. The limited inotropic response in severely failing human myocardium, together with possible vasorelaxation, may provide cardiac support in heart failure without an excessive increase in cardiac O2 demand.
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PMID:Calcium sensitization as a positive inotropic mechanism in diseased rat and human heart. 752 44

The authors describe the clinical characteristics and response to therapy of seven patients with hyperthyroidism, dilated cardiomyopathy, and low-output cardiac failure. All patients (4 women and 3 men, age 47 +/- 4 years, mean +/- standard error of the mean) were admitted with the primary diagnosis of congestive heart failure. The cause of hyperthyroidism was Graves' disease in six patients, and toxic multinodular goiter in one. On admission, the mean serum T4 was 21 +/- 1 microgram/dL and mean serum T3:411 +/- 77 ng/mL, and serum thyroid-stimulating hormone was suppressed ( < 0.03 microU/mL) in all patients. Two-dimensional echocardiogram showed biventricular or four chamber dilatation and impaired left ventricular performance. Therapy of heart failure and hyperthyroidism resulted in rapid clinical improvement. During follow-up (5 months to 9 years), left ventricular ejection fraction improved from a mean of 28% to a mean ejection fraction of 55% (P < 0.01). Resolution of dilated cardiomyopathy with normalization of systolic function was achieved in five patients, and improvement from severe to mild left ventricular dysfunction was observed in two patients. We conclude that some patients with hyperthyroidism may have a reversible form of dilated cardiomyopathy and "low-output failure." Assessment of thyroid hormone status in patients with heart failure might permit the identification of patients with dilated cardiomyopathy and thyrotoxicosis who are likely to have reversible cardia dysfunction.
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PMID:Congestive heart failure due to reversible cardiomyopathy in patients with hyperthyroidism. 766 12

A 24-year-old woman presented with right-sided infectious endocarditis due to methicillin-resistant Staphylococcus aureus (MRSA). This is the first report of right-sided infectious endocarditis caused by MRSA in Japan. The patient was admitted to the Jichi Medical School Hospital because of fever of unknown origin and disturbance of consciousness. Several months before, she had discontinued treatment for hyperthyroidism. Antibiotics effective against MRSA, vancomycin and flomoxef, were given intravenously, but a new heart murmur was detected. Echocardiographic study revealed vegetations attached to the tricuspid valve and abscess formation on the ventricular septum. The vancomycin dosage was increased and arbekacin sulfate was also given from the sixth hospital day. However, these antibiotics had very little effect and the abscess rapidly increased in size. Color flow mapping finally demonstrated intracardiac shunt flow through the ruptured abscess of the ventricular septum and sinus of Valsalva. She died suddenly, probably from heart failure. The prognosis of infectious endocarditis due to MRSA is poor and drug therapy often fails. Thus, surgery should be considered in the early stage.
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PMID:[Right-sided infectious endocarditis due to methicillin-resistant Staphylococcus aureus resulting in ruptured abscess of the ventricular septum and sinus of Valsalva]. 777 96

Coenzyme Q10 (CoQ10) plays an essential physiologic role in oxidative phosphorylation and its plasma and tissue concentration has been evaluated in various pathologic conditions, both endocrine and non endocrine; among the latter particularly in cardiac failure. Plasma CoQ10 determination has been reported in the literature an a useful diagnostic tool in differential diagnosis of thyroid diseases. In the present study we have evaluated CoQ10 circulating levels both in hypo- and hyperthyroidism. For this purpose plasma CoQ10, fT3-fT4 and TSH concentrations have been determined (HPLC, RIA and IRMA respectively) in a group of hypothyroid patients, hyperthyroid and control subjects. No patient was harbouring cardiovascular, metabolic or systemic disease. CoQ10 has resulted 0.97 +/- 0.46 mcg/ml in the hypothyroid group, 0.51 +/- 0.35 in hyperthyroid and 0.73 +/- 0.16 in control group, with a significative difference between first and second group only; more, the prevalence of high levels has appeared greater in hypo- towards hyperthyroid patients and that of low levels in the latter greater than in the former. Finally an inverse relation of CoQ10 with fT3 and tT3, but not with fT4 and tT4, has been shown. In conclusion, plasma CoQ10 levels have not given in this study a sharp distinction between euthyroidism on a side and hypo- and hyperthyroidism on the other, but necessity of longitudinal studies after therapy is outlined, both to know time of normalization of plasma concentrations and to verify the opportunity of exogenous administration of CoQ10 in hyperthyroid patients with risk factors for heart failure.
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PMID:[Circulating levels of CoQ10 in hypo- and hyperthyroidism]. 779 96

Heart function and plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA) and angiotension II (Ang II) were examined with echocardiography and radioimmunoassay in 9 patients with dilated cardiomyopathy (DCM), 41 with rheumatic heart disease (RHD), 29 with hyperthyroidism (Ht) and 24 normal subjects. ANP level was significantly increased as heart failure progressed (P < 0.01 and 0.001). There was negative correlation between ANP and left ventricular fractional shortening, and between ANP and ejection fraction in DCM and Ht groups. There was positive correlation between ANP and maximal left atrial diameter, right atrial area, and diastolic diameter or volume of left ventricle in DCM and RHD groups, and negative correlation between ANP and peak flow velocity in aorta or through mitral valve in DCM group (r = -0.608, P < 0.05 and r = 0.710, P < 0.05). These findings suggest that the stronger the myocardial contractility and the faster the blood flow, the lower the plasma ANP level.
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PMID:[Influence of cardiac structure, blood flow velocity and heart function on circulating atrial natriuretic peptide and renin-angiotension system]. 780 22

Two cases of high-output heart failure associated with pulmonary hypertension are presented. In a 32-year-old man with hyperthyroidism, pulmonary hypertension subsided after antithyroid therapy. Increased pulmonary blood flow and elevated left ventricular end-diastolic pressure were suspected as the causes of pulmonary hypertension. In a 51-year-old man with cardiac beriberi, the pulmonary hypertension improved after thiamine administration. We suspect that increased pulmonary blood flow, elevated left ventricular end-diastolic pressure, and probably pulmonary vasoconstriction were the causes of pulmonary hypertension. Thus, high-output heart failure should be considered as a possible cause of pulmonary hypertension and right ventricular failure.
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PMID:High-output heart failure as a cause of pulmonary hypertension. 791 25

Graves' disease, which is an organ-specific autoimmune disorder, is the most frequent cause of thyrotoxicosis. Females are more often affected than males. The clinical pattern varies, however, and nearly every organ system may be involved. This case study describes a formerly healthy young woman with Graves' disease who was admitted to the hospital with cardiac failure, convulsions and generalized lymphoid hyperplasia. A reversible thyrotoxic cardiomyopathia combined with hyperdynamic circulation may result in cardiac failure even in younger patients, and the cardiac function normalizes in the euthyroid state. Seizures may occur in association with hyperthyroidism. High doses of propranolol may precipitate the condition by lowering the threshold for seizures.
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PMID:[Heart failure and convulsions in thyrotoxicosis. A young woman with Graves' disease]. 797 5

Thyroid disease is common in veterinary practice. The heart, especially the myocardium, is sensitive to thyroid hormone, and deficiencies or excesses can alter cardiovascular function. Observed changes result from direct effects upon the myocardium and indirect effects that result from effects upon the vasculature and peripheral tissues. Clinically significant cardiovascular abnormalities related to hypothyroidism are rare. If present, they are primarily manifest as reduced left ventricular pump function, as apparent echocardiographically, or arrhythmias. Hyperthyroidism is common in the cat and infrequently encountered in dogs. Clinically significant cardiovascular manifestations are common and often dramatic. Hyperdynamic systolic function and mild myocardial hypertrophy are common manifestations which may lead to overt congestive and high output heart failure. If signs of congestive heart failure or significant arrhythmias are not evident, specific therapy need only be directed toward restoration of the euthyroid state. In most cases the cardiovascular changes associated with thyroid dysfunction are completely reversible.
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PMID:Effects of thyroid hormone and thyroid dysfunction on the cardiovascular system. 805 9

Platelet function, antithrombin and plasminogen activities, and fibrinolytic capabilities in 11 cats with acquired heart disease were compared with results in 4 healthy cats. Of 11 cats with heart disease, 9 had hyperthyroidism with secondary cardiac dysfunction. One cat with hyperthyroidism had renal disease and heart failure, and of 2 cats with idiopathic hypertrophic cardiomyopathy, 1 also had renal disease. At the time of testing, 3 cats had thromboembolic events associated with the disease. Compared with healthy cats, cats with acquired heart disease had increased activity of antithrombin III, a protein that behaves as an acute-phase reactant. Plasminogen activity was decreased, although not significantly, in cats with acquired heart disease, compared with results in healthy cats. In cats with left ventricular dysfunction, clot retraction was decreased (marginal significance, P = 0.058) and might be attributed, in some cases, to the medications received by the cats. Dilute whole blood clots from all cats failed to lyse in vitro. This observation, at present, lacks adequate explanation. Platelets from cats with acquired heart disease, compared with platelets from healthy cats, had decreased responsiveness (aggregation and [14C]serotonin release) to adenosine diphosphate and increased responsiveness to collagen. Hyperthyroid cats were receiving various drugs (propranolol, atenolol, or diltiazem) to empirically treat clinical signs of disease attributable to cardiac dysfunction. Although numbers of cats in each group were small, definite trends were observed in the results of tests. Platelets from cats receiving atenolol had decreased responsiveness to adenosine diphosphate and unaltered responsiveness to collagen, compared with platelets from healthy cats, and may have decreased risk of thrombus formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet function and antithrombin, plasminogen, and fibrinolytic activities in cats with heart disease. 806 8


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